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. 2022 Aug 13;41:244. doi: 10.1186/s13046-022-02457-4

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Aerobic glycolysis in NPC cells. LMP1 secreted by EBV enhances glucose consumption and lactate generation in NPC cells. Increased glucose consumption in the tumor cells leads to immune cell starvation. EBV (LMP1) leads to the accumulation of fumarate in the tricarboxylic acid cycle (TCA), which inhibits the expression of RIP3 and protects NPC cells from TNF-induced necrotizing apoptosis. GLUT1: glucose transporter 1, OAA: Oxaloacetic acid, a-KG: a–ketoglutarate, LDH: lactate dehydrogenase, G6PD: glucose-6-phosphate dehydrogenase